Rdiolipin or anti-2-glycoprotein-1 antibodies) were detected and his p…

Rdiolipin or anti-2-glycoprotein-1 antibodies) were detected and his plasma homocysteine level was normal. His fasting glucose (0.9 g/L) and hemoglobin A1C (4.7 ) levels, lipid profile (cholesterol: 1.8 g/L; high density cholesterol: 0.47 g/L; triglycerides: 1.6 g/L; low density cholesterol (Friedewald formula): 1.0 g/L) and liver function tests were also normal. Transesophageal echocardiography ruled out an emboligenic disease. Our patient was managed with aspirin, atenolol, captopril and atorvastatin but did not receive any anticoagulant treatment. He did not experience any angina recurrence. A submaximal exercise test on the sixth day was negative. An electrocardiogram on the seventh day (Figure 1B) showed a Q wave in inferior leads with apicolateral subepicardial ischemia. We did not detect any recurrence of the myocardial ischemia. A cardiac MRI performed one month after the acute episode identified a zone of myocardial necrosis and wall thinning, confirming the initial diagnosis (Figure 3).Discussion Afibrinogenemia and hypofibrinogenemia (in its isolated type; not associated with dysfibrinogenemia) are congenital quantitative abnormalities of fibrinogen. They expose patients to a bleeding risk of variable severity depending on their phenotype. Thrombotic complications, however, have been reported in the literature in isolated cases. These cases were venous [1] or arterialthromboses and most occurred after administration of cryoprecipitates or fibrinogen. Nevertheless, some cases of spontaneous arterial thrombotic events have been reported (Table 1). The majority of them concerned peripheral arteries in patients with afibrinogenemia (where fibrinogen levels are lower than those in patients with hypofibrinogenemia, leading to a more significant rise in the circulating thrombin, but it muct be noted that afibrinogenemia also has a greater prevalence). To the best of our knowledge, only a single case of myocardial infarction has previously been reported, in a 27year-old male patient with afibrinogenemia [2]. In our patient, in addition to the 8-Bromo-5-chloroquinoline typical clinical, ECG and biological features which were coherent with the definition of acute myocardial infarction, the diagnosis was further confirmed by MRI. Nevertheless, the coronary thrombosis was not viewed by a coronary computed tomography angiography (which was unavailable) or by invasive explorations, which were problematic in view of the hemorrhagic risk. For the patient described by Kumar et al. [2], who was admitted two hours after pain onset, as 3-[(Methylamino)methyl]phenol well as for our patient, who was admitted seven hours after pain onset, the risk of bleeding that accompanies coronary angioplasty (and its adjunctive anticoagulant therapy) seemed to outweigh the expected benefit and it was therefore not indicated in either case. PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/14704548 Also, because of the precarious balance of the process of hemostasis, thrombolytics and anti-thrombotic treatments could PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/12113769 not be used. The use of these treatments classically contraindicated in fibrinogen deficient patients has nevertheless been described in cases of thrombotic complications, often in parallel with fibrinogen infusion [3-5,10]. The increased risk of thrombosis in cases of fibrinogen deficiency could be explained by a rise in the level ofMghaieth et al. Journal of Medical Case Reports 2011, 5:582 http://www.jmedicalcasereports.com/content/5/1/Page 4 ofFigure 3 Long-axis image on contrast-enhanced inversion-recovery magnetic resonance performed one month after the a.